Is there an excess risk for colorectal cancer in patients with ulcerative colitis and concomitant primary sclerosing cholangitis? A population based study

Background—Patients with ulcerative colitis havean increased risk of colorectal cancer. Duration, age, and extent ofthe disease at diagnosis are the only established risk factors.Patients with ulcerative colitis and concomitant primary sclerosingcholangitis (PSC) have been reported to have a higher frequency ofcolonic DNA aneuploidy and/or dysplasia than expected, findingsindicating an increased risk of colorectal cancer compared with otherpatients with ulcerative colitis.
Methods—A population based cohort consisting of125 patients with a verified diagnosis of PSC was followed up bylinkage to the Swedish Cancer Registry for the occurrence of colorectal cancer.
Results—There were 12 colorectal cancers. Sixcancers were diagnosed prior to the diagnosis of PSC. Among the 104 patients with an intact colon at the time of the diagnosis of PSC there was a cumulative risk for colorectal cancer of 16% after 10 years. Among the 58 patients with a diagnosis of ulcerative colitis and colorectal cancer prior to the diagnosis of PSC, there were five colorectal cancers corresponding to a cumulative risk of 25% after 10years.
Conclusions—Patients with ulcerative colitis andconcomitant PSC seem to constitute a subgroup with a high risk forcolorectal cancer.

     

Acute "pseudo-angiocholitis" due to colonic adenocarcinoma in a man with primary sclerosis cholangitis and ulcerative colitis

We report the case of a 49-Year-old-man with primary sclerosis cholangitis (PSC) and ulcerative colitis who developed two acute episodes of pseudo-angiocholitis. Both episodes were triggered by septic hepatitis translocated from ulcerative colonic adenocarcinoma. The biliary MRI did not show any signs of lithiasis or cholangiocarcinoma. cholangiocarcinoma, intra-hepatic lithiasis and colonic cancer are potential diagnoses in patients with PSC who develop angiocholitis.     

Occurrence of dysplasia and adenocarcinoma after experimental chronic ulcerative colitis in hamsters induced by dextran sulphate sodium.

In this study, long term dextran sulphate sodium administration was studied to ascertain whether colorectal carcinoma could be produced in patients with long standing ulcerative colitis. Simultaneously, changes in the intestinal microflora were analysed. Low grade to high grade dysplasia was seen in three of the five hamsters treated with 1% dextran sulphate sodium solution for 100 days, while no dysplasia was detected in the eight animals concomitantly treated with metronidazole, an antianerobic microbial agent, which prevents colonic ulceration. In these two groups, none of the animals developed colorectal cancer over 100 day period. In a group treated for 180 days, seven of the eight animals had dysplasia, and one had two adenomas. Furthermore, four of the eight animals had adenocarcinoma in the transverse colon; they were protruding well differentiated adenocarcinoma in one and non-protruding lesions infiltrating into the musclaris propria in three. The three non-protruding infiltrating adenocarcinomas were classified to be well differentiated adenocarcinoma in one and mucinous adenocarcinoma in two, resembling the type of cancer which complicates ulcerative colitis in man.     

Ectopic colonic mucosa in ulcerative colitis and in Crohn's disease of the colon

Colectomy specimens from 62 patients (22 with ulcerative colitis, 20 with Crohn's disease of the colon, and 20 with invasive adenocarcinoma [without inflammatory bowel disease]) were reviewed for the presence of ectopic colonic mucosa. One or more foci of ectopic colonic mucosa were found in 16 of the 22 specimens (72 per cent) with ulcerative colitis and in 11 of the 20 specimens (55 per cent) with Crohn's disease of the colon. None of the 20 specimens having adenocarcinoma (without chronic inflammatory bowel disease) had ectopic colonic epithelium. The presence of ectopic colonic mucosa was found to be dependent on the age of the patients (more frequent among younger patients) and on the number of sections per specimen. One adenocarcinoma in a case of long-standing ulcerative colitis had apparently originated in ectopic colonic mucosa. This study was supported by grants from the Karolinska Institute.     

Colonic epithelial dysplasia or carcinoma in a regional group of patients with ulcerative colitis of more than 15 years duration

Colonoscopic screening for neoplasia was performed in a regional group of ulcerative colitis patients with a disease duration of greater than or equal to 15 years. A total of 121 patients, aged less than 80 years, were invited to participate, of whom 100 (83%) accepted colonoscopy, including biopsies in 15 standard locations of the entire colon, plus additional biopsies from all visible lesions. Unequivocal dysplasia was found in one patient with extensive colitis and a disease duration of 31 years. A polyp with highly differentiated adenocarcinoma was found in the sigmoid colon of a patient with intermittent rectum involvement, 37 years after the ulcerative colitis diagnosis had been made. Biopsy specimens from the remaining 98 patients showed no signs of dysplasia or cancer. Thus the frequency of pre-malignant or malignant changes is very low compared with the results of similar studies, and the rationale for general colonoscopic surveillance programmes for such patients is open to question.     

Ileostomy adenocarcinomas in the setting of ulcerative colitis

Adenocarcinomas arising at ileostomy sites in patients after colon resection for various diseases, such as ulcerative colitis (UC), familial adenomatous polyposis coli, and Crohn's disease, are rare occurrences but have been reported increasingly in the last 20 years. We report a case of adenocarcinoma arising in an ileostomy site in an 85-year-old woman with longstanding UC. She had pancolitis and underwent total proctocolectomy. Thirty-nine years later, her ileostomy site developed a granulation tissue-type lesion, which on initial biopsy revealed cytologic atypia in the presence of marked inflammation. A subsequent biopsy revealed adenocarcinoma with signet-ring cells and abundant extracellular mucin. Resection of the ileostomy was undertaken and a new ileostomy was performed. The literature on adenocarcinoma arising in the 23 patients with ulcerative colitis who received a Brooke or Kock ileostomy and had no prior history of neoplasm is reviewed.     

Adenocarcinoma below ileoanal anastomosis for ulcerative colitis: report of a case and review of the literature

BACKGROUND: Restorative proctocolectomy with hand-sewn ileoanal anastomosis and mucosectomy is warranted in patients with dysplasia and/or cancer on ulcerative colitis to prevent subsequent neoplastic changes in the retained mucosa. However, complete excision of the colonic mucosa cannot be obtained reliably. We report a case of anal canal adenocarcinoma after handsewn anastomosis with mucosectomy. METHODS: A 47-year-old patient, previously submitted to ileorectal anastomosis for colonic cancer on ulcerative colitis, underwent completion proctectomy and handsewn ileoanal anastomosis with mucosectomy for recurrent anastomotic cancer. Two years later, we submitted the patient to pouch removal with permanent ileostomy for a mucinous adenocarcinoma of the anal canal (T2N2Mx) found at follow-up pouch endoscopy. CONCLUSIONS: Only four cases of adenocarcinoma after handsewn anastomosis have been reported in the literature. This new case we report confirms that the risk of malignancy after ileoanal anastomosis with mucosectomy, although small, is real, despite the surgeon taking care with this particular step of the procedure. Careful surveillance is needed in patients with surgical treatment for long-term ulcerative colitis or dysplasia.     

A case of radiation-induced rectal cancer]

We report a case of radiation-induced rectal cancer, which is thought to originate from dysplasia due to radiation colitis. The patient is a 73 year-old woman, who underwent radical hysterectomy and radiotherapy for uterine cervical cancer 31 years ago. She visited to our hospital complaining of hematochezia. Colonoscopy in January 2004 disclosed redness of the rectal mucosa accompanied with contact bleeding and pathological study of the biopsy specimen revealed severe dysplasia. However, colonoscopy showed an ulcerative lesion of the rectum in December 2004, and pathological findings of the biopsy specimen disclosed moderately differentiated adenocarcinoma. She underwent a rectal resection in January 2005. Pathological study of resected specimen revealed fibrous change induced by radiation. Predominant histological type of the tumor was moderately differentiated carcinoma followed by well differentiated type. However, multiple dysplasias were found around the main tumor or in the mucosa which was treated with radiotherapy.     

Peptidergic nerves in the colon of patients with ulcerative colitis

BACKGROUND/AIMS: The cause of impaired motility, such as diarrhea and toxic megacolon, in patients with ulcerative colitis is unknown. Neuropeptides have recently been shown to be a neurotransmitter in the non-adrenergic non-cholinergic inhibitory and excitatory nerves in the human gut. To clarify the physiological significance of vasoactive intestinal polypeptide, substance P and neurotensin in the colon of patients with ulcerative colitis, we investigated the enteric nerve responses on lesional and normal bowel segments derived from patients with ulcerative colitis and patients who underwent colon resection for colonic cancers. METHODOLOGY: Twenty-four specimens were obtained from the lesional colon of 6 patients with ulcerative colitis (4 male, 2 female; ages 14-51 years, mean: 40.3 years). The patients with ulcerative colitis had chronic disease (4 with moderate disease, 2 with severe disease). Seventy-two specimens were obtained from the normal colon of 10 patients with colonic cancer (8 men and 2 women; ages 40-56 years, mean: 51.2 years). A mechanographic technique was used to evaluate in vitro muscle responses to these peptides of adrenergic and cholinergic nerves before and after treatment with various autonomic nerve blockers. RESULTS: (1) Peptidergic nerves such as vasoactive intestinal polypeptide, substance P, and neurotensin nerves were found to act on both normal colon and ulcerative colitis colon; (2) the colon with ulcerative colitis was more strongly innervated by vasoactive intestinal polypeptide nerves than the normal colon; (3) Substance P and neurotensin nerves act more weakly in the UC colon that the normal colon. CONCLUSIONS: These findings suggest that peptidergic nerves play an important role in the impaired motility observed in patients with UC.     

Dysplasia and cancer complicating strictures in ulcerative colitis

Previous studies have found a widely variable prevalence of dysplasia and cancer in colonic strictures in patients with ulcerative colitis. Consequently, therapeutic recommendations are conflicting. To better assess the prevalence, we reviewed the clinical and pathological findings in all 27 patients with ulcerative colitis complicated by stricture who were entered into our Inflammatory Bowel Disease Registry. A true stricture was defined as a persistant localized narrowing of the colon found on air-contrast barium enema or on colonoscopy. Upon careful review, 12 of 27 patients were found to have transient colonic spasm, not a stricture, and were excluded. The remaining 15 patients with true strictures represented 3.2% of all ulcerative colitis patients in the registry. Strictures were identified at 13.3± 9.9 years following the diagnosis of ulcerative colitis. Eleven patients had multiple strictures that were principally located in the left colon. Of the 15 patients, 11 had dysplasia and two had cancer found on colonoscopic biopsy. Ultimately, six patients had carcinoma found at colonoscopy or colectomy (three modified Dukes' stage A, one stage B, and two stage D). All cancers were at the site of a stricture. These findings indicate that a true colonic stricture in ulcerative colitis is frequently associated with dysplasia and cancer, which can be diagnosed with colonoscopic biopsy. A stricture should be considered a strong risk factor for cancer, requiring intensive colonscopic surveillance. If dysplasia is discovered, or if the stricture cannot be adequately biopsied, consideration should be given to total colectomy.Research supported by the David and Reva Logan Gastrointestinal Clinical Research Center and the Gastrointestinal Research Foundation Junior Board.     

Colorectal cancer in familial polyposis coli and ulcerative colitis

The records of all patients with familial polyposis coli and ulcerative colitis operated at The Mount Sinai Hospital were reviewed to determine the proportion of patients with cancer at the time of colon resection. Sixty-nine patients with familial polyposis coli undergoing operation between 1947 and 1983 were identified and 25 (36 percent) were found to have cancer. In the group with ulcerative colitis, 548 patients had surgical treatment between 1957 and 1983 and 65 (12 percent) had colonic cancer. There was a significant decrease in the proportion of patients with familial polyposis coli having cancer at the time of colon resection from 50 percent before 1968 to 20 percent since 1978. This change in cancer incidence was found to correlate with a decrease in the mean age at operation from 40 to 25 years. In the group with ulcerative colitis, the mean age at operation has remained essentially unchanged at 36 years. The proportion of patients with ulcerative colitis having cancer at the time of colon resection has remained constant throughout this study. Progression to carcinoma is still a significant concern in both familial polyposis coli and ulcerative colitis. Although removal of the colon and rectum prevents cancer development, patient selection and timing of the operation remain a difficult problem.     

Proximal colorectal dysplasia or cancer in ulcerative colitis. The impact of primary sclerosing cholangitis and sulfasalazine

PURPOSE: Known risk factors for the development of colorectal dysplasia or cancer in ulcerative colitis are total colonic involvement and long duration of the disease. It has recently been suggested that presence of primary sclerosing cholangitis is another independent risk factor—especially for proximal colorectal dysplasia or cancer—and that treatment with sulfasalazine might reduce the frequency of colorectal cancer in ulcerative colitis; the present study was undertaken to shed light on the validity of these theories. METHODS: A total of 143 patients with ulcerative colitis underwent regular colonoscopies and multiple biopsies in a 20-year surveillance program for studies of long-standing total ulcerative colitis. Fifty-one of the patients developed colorectal dysplasia or cancer. Patient records were scrutinized retrospectively for information of presence of primary sclerosing cholangitis, site of the colorectal malignancy, and results of sulfasalazine treatment. RESULTS: Nineteen of the patients had primary sclerosing cholangitis; these ran a significantly higher risk of developing colorectal dysplasia or cancer than patients with ulcerative colitis only. All colorectal cancers (n=3) and 75 percent of all colorectal dysplasias or cancers among patients with primary sclerosing cholangitis were located in the proximal part of the colon, whereas 36 percent were found in that same region among the patients with ulcerative colitis without primary sclerosing cholangitis (P=0.02). Sulfasalazine treatment showed no significant protective effect on the development of colorectal dysplasia or cancer in patients with ulcerative colitis. CONCLUSION: The risk evaluation, as assessed by multivariate analysis, shows that primary sclerosing cholangitis proves to be an additional and independent risk factor for the development of colorectal dysplasia or cancer in patients with ulcerative colitis—particularly in the proximal part of the colon. The findings do not support the theory that sulfasalazine treatment exerts a protective effect against colorectal dysplasia or cancer.     

Proximal colorectal dysplasia or cancer in ulcerative colitis. The impact of primary sclerosing cholangitis and sulfasalazine: results from a 20-year surveillance study.

PURPOSE: Known risk factors for the development of colorectal dysplasia or cancer in ulcerative colitis are total colonic involvement and long duration of the disease. It has recently been suggested that presence of primary sclerosing cholangitis is another independent risk factor-especially for proximal colorectal dysplasia or cancer-and that treatment with sulfasalazine might reduce the frequency of colorectal cancer in ulcerative colitis; the present study was undertaken to shed light on the validity of these theories. METHODS: A total of 143 patients with ulcerative colitis underwent regular colonoscopies and multiple biopsies in a 20-year surveillance program for studies of long-standing total ulcerative colitis. Fifty-one of the patients developed colorectal dysplasia or cancer. Patient records were scrutinized retrospectively for information of presence of primary sclerosing cholangitis, site of the colorectal malignancy, and results of sulfasalazine treatment. RESULTS: Nineteen of the patients had primary sclerosing cholangitis; these ran a significantly higher risk of developing colorectal dysplasia or cancer than patients with ulcerative colitis only. All colorectal cancers (n = 3) and 75 percent of all colorectal dysplasias or cancers among patients with primary sclerosing cholangitis were located in the proximal part of the colon, whereas 36 percent were found in that same region among the patients with ulcerative colitis without primary sclerosing cholangitis (P = 0.02). Sulfasalazine treatment showed no significant protective effect on the development of colorectal dysplasia or cancer in patients with ulcerative colitis. CONCLUSION: The risk evaluation, as assessed by multivariate analysis, shows that primary sclerosing cholangitis proves to be an additional and independent risk factor for the development of colorectal dysplasia or cancer in patients with ulcerative colitis-particularly in the proximal part of the colon. The findings do not support the theory that sulfasalazine treatment exerts a protective effect against colorectal dysplasia or cancer.     

Ursodiol use is associated with lower prevalence of colonic neoplasia in patients with ulcerative colitis and primary sclerosing cholangitis

BACKGROUND: Patients with ulcerative colitis and primary sclerosing cholangitis are at high risk for colonic dysplasia and cancer. This risk approaches 50% after 25 years of colitis. Ursodiol has been shown to protect against development of colorectal neoplasia in animal models. OBJECTIVE: To assess the relationship between ursodiol use and colonic dysplasia, the precursor to colon cancer, in patients with ulcerative colitis and primary sclerosing cholangitis. DESIGN: Cross-sectional study. SETTING: University medical center. PATIENTS: 59 patients with ulcerative colitis and primary sclerosing cholangitis who were undergoing colonoscopic surveillance for colonic dysplasia. MEASUREMENTS: Use of ursodiol was assessed in all patients. The presence or absence of colonic dysplasia was evaluated by colonoscopic surveillance. Other variables assessed were age at onset and duration of ulcerative colitis; duration of primary sclerosing cholangitis; Child-Pugh classification; and use of sulfasalazine, other 5-aminosalicylic acid preparations, prednisone, cyclosporine, azathioprine, and methotrexate. RESULTS: Ursodiol use was strongly associated with decreased prevalence of colonic dysplasia (odds ratio, 0.18 [95% CI, 0.05 to 0.61]; P = 0.005). The association between dysplasia and ursodiol use remained after adjustment for sex, age at onset of colitis, duration of colitis, duration of sclerosing cholangitis, severity of liver disease, and sulfasalazine use (adjusted odds ratio, 0.14 [CI, 0.03 to 0.64]; P = 0.01). Younger age at onset of colitis was associated with an increased risk for dysplasia. CONCLUSIONS: Ursodiol use appears to be associated with a lower frequency of colonic dysplasia in patients with ulcerative colitis and primary sclerosing cholangitis. A randomized trial investigating the chemoprotective effect of ursodiol in patients with ulcerative colitis may be warranted.     

Colorectal Carcinomas Following Ulcerative Colitis in Japanese Patients

Abstract: Colorectal carcinomas occuring following ulcerative colitis in Japanese patients discussed in the literature were analyzed in order to review their characteristics. 1) Of the 74 cases reported from 1962 to November 1989, 29 were males and 45 were females. The sex differences in Japanese ulcerative colitis were almost 1: 1, so females with colorectal carcinomas occured more often than males. 2) Male patients had a bimodal peak in their 30's and 40's, while female patients had the peak in their 40's and 50's. More colorectal carcinomas were found among younger people than in the general population. 3) Universal colitis was the most common type of colorectal cancer occuring following ulcerative colitis. 57 patients out of 74 were classified into this type. 4) The duration of the disease prior to the diagnosis of colorectal cancer was generally 10 years or longer. 5) The rectum was the commonest site of cancer, and was seen in 44 cases out of 74. Rectosigmoid colon carcinomas occurred in 61 of 74 cases. 6) Histologically, colonic malignancy associated with ulcerative colitis was an adenocarcinoma, displaying a wide spectrum of differentiation. Poorly differentiated (4 males and 6 females) and signet ring cell carcinoma (3 males and 5 females) were also reported. 7) The so-called type 4 tumor occurred in 3 males and 6 females out of a total of 74 cases. This type of tumor is usually rare in colorectal cancer. 8) Most of the patients with early carcinomas had suffered from ulcerative colitis for more than 15 years and the characteristics of their macroscopic appearance were protruded lesions. 9) Foci of dysplasia accompanied carcinoma in as many as 80% of the Japanese cases reported. (56 out of 74 cases) Based on these, we should take consideration that: 1) Patients with pancolitis lasting more than 10 years whose forms are chronically active or intermittently active should be recognized as a high-risk group. 2) Full colonoscopy every one or two years may be sufficient to find dysplasia as well as carcinoma even if the condition of disease is stable. 3) Protruded lesions should be biopsied to detect early cancer as well as dysplasia on colonoscopy. 4) A change in the disease condition, i. e. rectal bleeding, weight loss and a change of bowel habits should not be mistaken for an exacerbation of colitis and should be investigated without fail.     

Association between CYP24A1 polymorphisms and the risk of colonic polyps and colon cancer in a Chinese population

AIM To determine the pathogenesis and potential single nucleotide polymorphisms(SNPs) as screening sites for colonic polyps,colon cancer and ulcerative colitis,and to analyze the possible association between these genetic polymorphisms and the three diseases. METHODS We evaluated genetic polymorphisms in 144 newly diagnosed colonic polyp patients,96 colon cancer patients and 44 ulcerative colitis patients. The four SNPs genotyped were rs4809957,rs6068816,rs6091822 and rs8124792. The control group consisted of 504 East Asians enrolled in the 1000 Genomes Project. Correlations between CYP24A1 SNPs and the diseases were analyzed by Fisher's exact probability test.RESULTS CYP24A1 polymorphisms rs4809957 A/G and rs6068816 C/T showed a statistically significant association with risk of the three diseases,when both the genotypes and allele frequencies were considered. With regard to rs6091822 G/T,all three diseases were related to risk allele carriers(GT + TT) vs wild-type(GG),but the associations between the allele frequencies and the diseases were not significant. The risk of colonic polyps and colon cancer was related to the allele frequencies of rs8124792 G/A,and this association remained for genotype frequencies of this SNP. CONCLUSION Four SNPs are related to the risk of colonic polyps and colon cancer. G allele in rs6091822 G/T may play an anti-cancer role only if it is homozygous. The A allele,which is a minor component of rs8124792,may be indicated in the diagnosis of colonic polyps or colon cancer rather than ulcerative colitis.     

Early gallbladder carcinoma associated with primary sclerosing cholangitis and ulcerative colitis

Patients troubled with primary sclerosing cholangitis (PSC) and ulcerative colitis (UC) are at high risk for cholangiocarcinoma, whereas cancer of the gallbladder (GBC) is rarely reported to develop in that population. A Japanese man aged 62 years with a 14-year history of PSC and UC had been found to have a protruding lesion of the gallbladder by screening sonography. The preoperative examination suggested the lesion to be GBC at an early stage. Pathology examination after cholecystectomy proved that the lesion was papillary adenocarcinoma localized in the mucosal layer. Although the prognosis of GBC is poor, the outcome of cholecystectomy against early GBC is relatively good. Early detection of the tumor is required for a better prognosis of patients with GBC. According to the review of the literature, PSC and UC patients are regarded as a high-risk group not only for cholangiocarcinoma but also GBC. It is advocated that clinicians perform repeated radiographic examinations including sonography for patients with PSC and UC even if the diseases are being controlled.     

Managing the cancer risk in chronic ulcerative colitis. A decision-analytic approach

Chronic ulcerative colitis is associated with a high risk of colon cancer. The most appropriate management--prophylactic proctocolectomy or medical surveillance--is, at present, unclear. Recent reports suggest that the presence of colonic dysplasia or "precancer" on endoscopic biopsy may be a reliable predictor of concurrent or future colon cancer. To assess the value of colonic dysplasia in managing colitis patients, I applied decision analytic techniques to currently available data regarding the sensitivity and specificity of colonic dysplasia in colitis patients. Such analysis shows that management based on biopsy for colonic dysplasia, rather than prophylactic proctocolectomy for all colitis patients, will maximize 5-year survival. Sensitivity analysis suggests that management is primarily determined by the sensitivity of biopsy-diagnosed dysplasia--elective prophylactic surgery would be preferred only when sensitivity of dysplasia on biopsy is less than or equal to 0.70 at 20 years, or less than or equal to 0.85 at 30 years of colitis, and changing surgical mortality and survival benefit from early diagnosis within a range established by previous studies affects management decisions only when sensitivity of dysplasia is at the lower end of its reported range.     

Microsatellite Instability Is Uncommon in Intestinal Mucosa of Patients with Crohn's Disease

Patients with long-standing inflammatory bowel disease have an increased risk for colorectal carcinoma. Microsatellite instability occurs in colonic neoplasms and has been reported in colonic tissues from patients with ulcerative colitis. Patients with Crohn's disease also have an increased risk for colorectal cancer, although it is lower than that associated with ulcerative colitis. This study was designed to determine whether microsatellite instability occurs in Crohn's disease, and whether it occurs with similar frequency to that observed in ulcerative colitis. In all, 177 tissue samples from 33 patients with Crohn's disease were evaluated for microsatellite alterations. Microsatellite instability occurred in five different tissue samples from one of 33 Crohn's disease patients. Four of the five tissue samples showed microsatellite instability at more than one locus. We conclude that microsatellite instability is less common in Crohn's disease than ulcerative colitis and may reflect differences in cancer risk between these two forms of inflammatory bowel disease.     

Failure of colonoscopic surveillance in ulcerative colitis.

A prospective surveillance programme for patients with longstanding (> = 8 years), extensive (> = splenic flexure) ulcerative colitis was undertaken between 1978 and 1990. It comprised annual colonoscopy with pancolonic biopsy. One hundred and sixty patients were entered into the programme and had 739 colonoscopies (4.6 colonoscopies per patient; 709 patient years follow up). Eight eight per cent of examinations reached the right colon. There was no procedure related death. One Dukes's A cancer was detected. Forty one patients (25%) defaulted. Of these 25 remain well; 13 are unaccounted for, and one died from colonic cancer. One patient had colectomy for medical reasons, and another died of carcinoma of the pancreas. Retrospectively an additional 16 eligible patients were identified who had not been recruited. Of these, 14 remain well, two are unaccounted for. None developed colonic cancer. Four patients refused colonoscopy. All remain well. Over the same period seven other cases of colonic cancer were found in association with ulcerative colitis, two in patients who had erroneously been diagnosed as having only proctitis and were therefore not entered into the programme, but were found at operation to have total colitis, one in a patient with colitis of seven years duration, and four patients who had previously attended the clinic but had been lost to follow up before 1978 and then had represented with new symptoms during the surveillance period. Thus, of the nine colitis related cancers diagnosed in this centre during the study period only one was detected by the surveillance programme. The results of this large study, a a review of published works, cast doubts on the effectiveness of colonoscopic surveillance programmes in detecting colorectal cancer in patients with ulcerative colitis.